We have found that inhibition of the MAPK p38 in sea urchin embryos results in the disruption of larval skeletal patterning. Patterning involves the interaction of ectoderm and mesoderm, but the mechanism and molecular details are unknown in this and other patterning models, such as the vertebrate limb or the insect imaginal disc. In Aim 1, we will assess whether patterning cues within the ectoderm are local or global by expressing p38 mutants in restricted ectodermal regions. In Aim 2, we will characterize the interaction of ectoderm and mesoderm, and assess the contribution of thin filopodia to the transduction of patterning signals. In Aim 3, we will identify proteins involved in patterning through the use of subtractive hybridization. Together, the results of this study will define the molecules and mechanisms underlying embryonic pattern formation in a simple model system.